PUBLICATION
            Kctd12 and Ulk2 partner to regulate dendritogenesis and behavior in the habenular nuclei.
- Authors
- Lee, S., Page-McCaw, P., Gamse, J.T.
- ID
- ZDB-PUB-150902-1
- Date
- 2014
- Source
- PLoS One 9(10): 1-7 (Journal)
- Registered Authors
- Gamse, Josh, Page-McCaw, Patrick
- Keywords
- Neuronal dendrites, embryos, larvae, zebrafish, neuronal morphology, neurons, behavior, morpholino
- MeSH Terms
- 
    
        
        
            
                - Protein Serine-Threonine Kinases
- Habenula/cytology*
- Habenula/growth & development
- Animals
- Nerve Tissue Proteins/metabolism*
- Cation Transport Proteins/metabolism*
- Protein Structure, Tertiary
- Environment
- Gene Knockdown Techniques
- Anxiety/metabolism
- Anxiety/pathology
- Zebrafish/growth & development
- Zebrafish/metabolism
- Zebrafish Proteins/chemistry
- Zebrafish Proteins/deficiency
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- Behavior, Animal*
- Dendrites/metabolism*
 
- PubMed
- 25329151 Full text @ PLoS One
            Citation
        
        
            Lee, S., Page-McCaw, P., Gamse, J.T. (2014) Kctd12 and Ulk2 partner to regulate dendritogenesis and behavior in the habenular nuclei.. PLoS One. 9(10):1-7.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                The habenular nuclei of the limbic system regulate responses, such as anxiety, to aversive stimuli in the environment. The habenulae receive inputs from the telencephalon via elaborate dendrites that form in the center of the nuclei. The kinase Ulk2 positively regulates dendritogenesis on habenular neurons, and in turn is negatively regulated by the cytoplasmic protein Kctd12. Given that the habenulae are a nexus in the aversive response circuit, we suspected that incomplete habenular dendritogenesis would have profound implications for behavior. We find that Ulk2, which interacts with Kctd12 proteins via a small proline-serine rich domain, promotes branching and elaboration of dendrites. Loss of Kctd12 results in increased branching/elaboration and decreased anxiety. We conclude that fine-tuning of habenular dendritogenesis during development is essential for appropriate behavioral responses to negative stimuli.
            
    
        
        
    
    
    
                
                    
                        Errata / Notes
                    
                    
                
                
            
        
        
    
        
            
            Correction to this article: 3 Feb 2015: The PLOS ONE Staff (2015) Correction: Kctd12 and Ulk2 Partner to Regulate Dendritogenesis and Behavior in the Habenular Nuclei. PLoS ONE 10(2): e0117637. doi: 10.1371/journal.pone.0117637
        
        
    
    
    
                
                    
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